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Clin Med II > Dermatology with no pictures > Flashcards

Dermatology with no pictures Flashcards

1
Q

What are the two types of skin diseases?

A
  1. Growth

2. Rash

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2
Q

What is a growth?

A

a cyst, a malformation, or a benign or malignant neoplasm

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3
Q

What is a rash?

A

an inflammatory skin condition or a dermatitis

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4
Q

List the Eczematous Eruptions.

A 
1. Atopic Dermatitis
(Eczema)
2. Contact Dermatitis (2)
3. Allergic contact dermatitis
4. Nummular Eczema
5. Seborrheic Dermatitis
6. Perioral Dermatitis
7. Stasis Dermatitis
8. Pompholyx: Vesiculobullous Hand Eczema (formerly 
Dyshidrosis Eczema)
9. Lichen Simplex Chronicus
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5
Q

What is Atopic Dermatitis (Eczema)

A

Acute, subacute, or chronic relapsing skin disorder that usually begins in infancy (rarely adult) and is characterized principally by dry skin and pruritus

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6
Q

During your Derm rotations, your preceptor mentions “The itch that rashes”–what is she referring to?

A

Atopic Dermatitis (Eczema)

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7
Q

Is Atopic Dermatitis IgE or IgA mediated?

A

IgE mediated

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8
Q

Atopic Dermatitis: “Itch-Scratch” cycle –> ?

A

lichenification

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9
Q

What are some eliciting factors for Atopic dermatitis?

A
  1. Inhalants (dust mites and pollens)
  2. Microbial Agents (exotoxins of Staphylococcus aureus)
  3. Foods (eggs, milk, peanuts, soybeans, fish, and wheat)
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10
Q

A decrease of barrier function, water loss by frequent bathing and hand washing; dehydration is an important exacerbating factor of what? In what specific condition?

A
  1. Skin barrier disruption

2. Atopic dermatitis

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11
Q

T/F: Infections from S. aureus can be an exacerbating factor for Atopic dermatitis?

A

True

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12
Q

A patient comes in complaining of urticarial outbreaks in the winter. She says the bursts

A

Winter is an exacerbating factor for atopic dermatitis

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13
Q

A patient comes in complaining of urticarious flares that always arise when she is taking off her wool coat–what is the most likely offending agent?

A

Atopic dermatitis

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14
Q

A patient comes in complaining of a “rash”–he describes the rash as red then turned to small bumps and bigger bumps with flaking. You inspect the area and note xerosis, cracks, fissures and excoriations. What is this patients likely diagnosis?

A

ACUTE Atopic Dermatitis

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15
Q

What is the difference between acute and chronic atopic dermatitis?

A

Lichenification

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16
Q

A mother brings in her child; you note the flaking and erythema on the face and trunk of the infant. What is the likely diagnosis of this “rash”?

A

Atopic dermatitis

-presents in the face and trunk of babies

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17
Q

A worried father brings in his son with a “flaking red rash.” You inspect the rash and note the rash’s distribution is mixed showing up on the face, trunk. and flexural areas. You ask when this rash began and the father replies if was after taking the boys wool coat off. What is the most likely offending agent?

A

Atopic Dermatitis

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18
Q

A 30 year old patient comes in complaining of a “red itchy rash” on her arms and legs. She replies it occurred right after her boyfriend broke up with her. What do you suspect is the cause of the rash?

A

Emotional stress triggered Atopic Dermatitis

-presents on the flexural areas on the adult

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19
Q

What is the treatment for ACUTE Atopic Dermatitis?

A

Acute Tx

  • Wet dressings, topical glucocorticoids
  • Hydroxyzine 10 – 100 mg QID
  • Oral antibiotics (dicloxacillin or erythromycin) to eliminate S. aureus
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20
Q

Should a patient with Atopic Dermatitis be scratching?

A

NO!!!!

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21
Q

What is the treatment for SUBACUTE/CHRONIC Atopic Dermatitis?

A

Subacute/Chronic

  • Hydration + emollients
  • topical glucocorticoids
  • Tacrolimus or pimecrolimus
  • H1 antihistamines
  • UVA-UVB therapy
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22
Q

What is Contact Dermatitis?

A

Acute or chronic inflammatory reactions to substances that come in contact with the skin

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23
Q

What are the 2 types of Contact Dermatitis?

A
  1. Irritant contact dermatitis

2. Allergic contact dermatitis

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24
Q

A patient comes in complaining of a “chemical rash” on his hands. What is the most likely diagnosis?

A

Irritant contact dermatitis

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25
Q

What causes Allergic contact dermatitis?

A

caused by an antigen (allergen) that elicits a type IV (cell-mediated or delayed) hypersensitivity reaction

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26
Q

What si the Pathogenesis of Irritant contact dermatitis (ICD)?

A
  • defense or repair capacity altered

- chemical induced inflammatory response

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27
Q

A patient comes in complaining of burning, tingling and “smarting” rash on his hands. What is most likely the diagnosis?

A

Irritant contact dermatitis

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28
Q

This is a description of which skin lesion?

Erythema with a dull, non glistening surface –> vesiculation–> erosion crusting–> shedding of crusts and scaling

A

Irritant contact dermatitis (non-chemical burn)

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29
Q

Describe a skin lesion of Irritant Contact Dermatitis in a chemical burn.

A

Erythema–> necrosis–> shedding of necrotic tissue–> ulceration–> healing

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30
Q

In what situations is ICD chronic?

A
  • Cumulative (mild irritants

- Irritant reaction (wet work)

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31
Q

What is the Treatment for ICD?

A
  • Avoidance of irritant
  • Wet dressings – Burow’s solution
  • Topical/Oral Steroids
  • Lubricating/protective creams/ointments
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32
Q

How do you investigate allergic contact dermatitis?

A

with Patch testing

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33
Q

What type of hypersensitivity reaction is allergic contact dermatitis?

A

Type IV

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34
Q

What does the appearance of Allergic Contact Dermatitis depend on?

A

Severity
Location
Duration

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35
Q

What do the skin lesions of Allergic Contact Dermatitis look like?

A
  • Well demarcated, erythema, inflamed, swollen areas
  • Papules, dry scales
  • Vesicular and bullous
  • Exudative and crusty
  • Often linear
  • Itchy
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36
Q

While inspecting a patient, you notice a well demarcated, erythematous, inflamed, swollen area on the arm. There are papules, and signs of dry scales. On the opposite arm you note vesicles and bullae that are exudative and crusty. The “rash” seems linear. The patient reports itchiness. What is the most likely diagnosis?

A

Allergic Contact Dermatitis

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37
Q

While inspecting a patient, you notice a well demarcated, erythematous, inflamed, swollen area on the arm. There are papules, and signs of dry scales. On the opposite arm you note vesicles and bullae that are exudative and crusty. The “rash” seems linear. The patient reports itchiness. What is the best treatment option?

A
  • Identify and remove agent
  • Topical glucocorticoid ointments/gels (acute, nonbullous)
  • Prednisone 70 mg 1-2 weeks (severe)
  • Drain vesicles but do not remove top
  • Wet dressings with cloths soaked in Burow’s solution changed every 2 to 3 h
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38
Q

What is Nummular Eczema?

A
  • chronic, pruritic, inflammatory dermatitis
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39
Q

A patient comes in complaining of “coin-shaped” plaques composed of grouped small papules and vesicles on an erythematous base. You ask about history but the patient says nothing out of the ordinary except that this same “rash” occurred last winter as well. What is the most likely diagnosis?

A

Nummular Eczema

cause unknown

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40
Q

A patient comes in complaining of “coin-shaped” plaques composed of grouped small papules and vesicles on an erythematous base. You ask about history but the patient says nothing out of the ordinary except that this same “rash” occurred last winter as well. What is the best option for treatment?

A
  • Skin hydration – Moisturize
  • Glucocorticoids
  • Crude Coal tar - 2 to 5% crude coal tar ointment daily.
  • Systemic Therapy - antibiotics if S. aureus is present.
  • PUVA or UVB 311-nm therapy
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41
Q

“Dandruff” or “Cradle cap”

A

Seborrheic Dermatitis

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42
Q

Cause of “Dandruff” or “Cradle cap”?

A

fungal, B6 and Zn deficiencies, cradle cap - unknown

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43
Q

“Dandruff” or “Cradle cap”–> SEVERE??

A

Think HIV

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44
Q

What is Seborrheic Dermatitis?

A

Redness and scaling and occurring in regions where the sebaceous glands are most active
(scalp, gluteal crease, neck line, breast, face)

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45
Q

A patient walk in with orange-red or gray-white skin, “greasy” or white dry scaling macules and papules of varying size. The rash is sharply marginated
with sticky crusts and fissures in the folds behind the external ear. On the scalp you note scaling (“dandruff”). The face and trunk have scattered scaling. On the trunk there are
nummular, polycyclic, and even annular spots. Overall you notice diffuse involvement of scalp. What is the most likely diagnosis?

A

Seborrheic Dermatitis

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46
Q

A patient walk in with orange-red or gray-white skin, “greasy” or white dry scaling macules and papules of varying size. The rash is sharply marginated
with sticky crusts and fissures in the folds behind the external ear. On the scalp you note scaling (“dandruff”). The face and trunk have scattered scaling. On the trunk there are
nummular, polycyclic, and even annular spots. Overall you notice diffuse involvement of scalp. What is the most appropriate treatment?

A
  • Selenium sulfide (Selsun Blue) or zinc pyrithione (Head & Shoulders) shampoos
  • Ketaconazole shampoo (Nizoral OTC????, prescription 2%)
  • Mineral oil/Baby oil/Olive oil
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47
Q

What is Perioral Dermatitis?

A

Discrete erythematous micropapules and microvesicles

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48
Q

What population does Perioral Dermatitis effect?

A

Young women (16 – 45 years old)

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49
Q

An 18 year old female patient comes in complaining of tiny red bumps around her mouth. How long do you tell her this will last?

A

Duration: weeks to months

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50
Q

An 18 year old female patient comes in complaining of tiny red bumps around her mouth. What do you explain as the most likely causative agent?

A

Unknown

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51
Q

An 18 year old female patient comes in complaining of tiny red bumps around her mouth. What do you treat this patient with?

A
  • Avoid topical steroids
    1. Topical
    • Metronidazole 0.75% cream BID or 1% QD
  1. Systemic
    • Minocycline or Doxycycline 100 mg QD until clear, then 50 mg QD x 2 months or
    • Tetracycline 500 mg BID until clear, 500 mg QD x 1 month , then 250 mg QD x 1 month
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52
Q

A 40 yr old male truck driver comes to your office complaining of a “rash” on his legs. You inspect and find: Eczematous dermatitis w/inflammatory papules, scaly and crusted erosions, excoriations, sclerosis, pigmentation. What is the most likely cause?

A

Venous Insufficiency

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53
Q

A 40 yr old male truck driver comes to your office complaining of a “rash” on his legs. You inspect and find: Eczematous dermatitis w/inflammatory papules, scaly and crusted erosions, excoriations, sclerosis, pigmentation. What is the most appropriate treatment?

A
  • Topical glucocorticoids (short term)
  • Topical antibiotics (mupirocin) 2ndary infection
  • Culture for MRSA?
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54
Q

Vesicular type of hand and foot dermatitis

A

Pompholyx: Vesiculobullous Hand Eczema (formerly Dyshidrosis Eczema)

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55
Q

While inspecting a patient you notice deep-seated pruritic, clear “tapioca-like” vesicles. If left untreated, what can you expect this rash to look like?

A

Later, scaling fissures and lichenification occur–there will also be recurrent attacks

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56
Q

While inspecting a patient you notice deep-seated pruritic, clear “tapioca-like” vesicles. What needs to be done in order to properly treat this patient?

A

R/O bacterial or fungal cause

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57
Q

While inspecting a patient you notice deep-seated pruritic, clear “tapioca-like” vesicles. You rule out any bacterial or fungal causes. What is the proper treatment?

A
  • Topical and Systemic corticosteroids
  • Intralesional injection – Triamcinolone
  • Systemic – tapered prednisone
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58
Q

While inspecting a patient you notice deep-seated pruritic, clear “tapioca-like” vesicles. You rule out any bacterial or fungal causes. What is the most likely diagnosis?

A

Pompholyx: Vesiculobullous Hand Eczema (formerly Dyshidrosis Eczema)

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59
Q

Localized form of lichenification, it results from repetitive rubbing and scratching

A

Lichen Simplex Chronicus

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60
Q

What population does Lichen Simplex Chronicus most commonly effect?

A

Individuals older than 20 years, more frequent in women, and possibly more frequent in Asians

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61
Q

What is the pathogenesis of Lichen Simplex Chronicus?

A
  1. Physical trauma = skin hyperplasia
  2. Emotional stress
  3. Habit forming/unconscious habit
  4. “Pleasure habit”
  5. Itch attack from minor stimuli
  6. (nervousness, anxiety, depression and other psychological disorders?)
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62
Q

While inspecting a patient, you notice a solid plaque of lichenification, arising from small papules; the scaling is minimal except on the lower extremities.
The lichenified skin is palpably thickened. Excoriations are noted. Dull red, and brown and black hyper pigmentation are also noted. Round, oval, linear rash, sharply defined. What is the most likely diagnosis?

A

Lichen Simplex Chronicus

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63
Q

While inspecting a patient, you notice a solid plaque of lichenification, arising from small papules; the scaling is minimal except on the lower extremities.
The lichenified skin is palpably thickened. Excoriations are noted. Dull red, and brown and black hyper pigmentation are also noted. Round, oval, linear rash, sharply defined. What is the most likely cause?

A

repetitive rubbing and scratching

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64
Q

While inspecting a patient, you notice a solid plaque of lichenification, arising from small papules; the scaling is minimal except on the lower extremities.
The lichenified skin is palpably thickened. Excoriations are noted. Dull red, and brown and black hyper pigmentation are also noted. Round, oval, linear rash, sharply defined. What is the treatment?

A
  • Difficult to treat
  • Stop scratching or rubbing!
  • Topical glucocorticoid preparations or tar preparations + occlusive dressings
  • Intralesional triamcinolone
  • Oral hydroxyzine (night)
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65
Q

Acute or chronic inflammatory dermatosis involving skin and/or mucous membranes

A

Lichen planus

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66
Q

What population does Lichen plants usually affect?

A

Age of onset - 30 to 60 years, F > M

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67
Q

What is the cause of Lichen Planus?

A
  • Idiopathic (most cases)

- Cell-mediated immunity (lymphocytes) plays a major role

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68
Q

What are some of the drugs that cause Lichen Planus?

A

viral (Hep C), metals (gold, mercury)

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69
Q

T/F: Lichen Planus is HLA-associated.

A

True

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70
Q

What is the difference between Acute and Chronic Lichen Planus?

A

Acute: onset lasts for days
Chronic: onset lasts over weeks

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71
Q

Four P’s—papule, purple, polygonal, pruritic

A

Lichen Planus

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72
Q

How can you expect to see Lichen Planus in dark-skinned individuals?

A

Postinflammatory hyperpigmentation (PIH) is common

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73
Q

While inspecting a patient, you note papules, flat-topped, 1 to 10 mm, sharply defined, shiny
violaceous, with white lines (Wickham’s striae). What is missing to complete the picture when Lichen Planus is generalized?

A
  • Polygonal or oval.

- Grouped, linear, annular, or disseminated scattered discrete lesions when generalized

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74
Q

While inspecting a patient, you note papules, flat-topped, 1 to 10 mm, sharply defined, shiny
violaceous, with white lines (Wickham’s striae). What is the most likely diagnosis?

A

Lichen Planus

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75
Q

While inspecting a patient, you note papules, flat-topped, 1 to 10 mm, sharply defined, shiny
violaceous, with white lines (Wickham’s striae). Where can you expect to see this rash on the body?

A

Wrists (flexor), lumbar, shin, scalp, and mouth

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76
Q

While inspecting a patient, you note papules, flat-topped, 1 to 10 mm, sharply defined, shiny
violaceous, with white lines (Wickham’s striae). What is the treatment?

A
  • Topical or Systemic glucocorticoids
  • Cyclosporine or Tacrolimus soln.
  • PUVA
  • Systemic Retinoids
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77
Q

Acute exanthematous eruption with a distinctive morphology and often self-limited course

A

Pityriasis rosea

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78
Q

What is the most common population that Pityriasis rosea effects? What time of year does this usually happen?

A
  • Age of onset - 10 to 43 years

- Season - Spring and fall.

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79
Q

What is the most likely cause of Pityriasis rosea?

A

Etiology – HHV 6 or 7 reactivation

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80
Q

One of your patients has just been recently diagnosed with Pityriasis Rosea. She wants to know how long this will last and if this is lifelong. What do you tell her?

A
  • Duration – a single herald patch precedes the exanthematous phase; which develops over a period of 1 to 2 weeks
  • Spontaneous remission in 6 to 12 weeks or less
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81
Q

80% of patients have this:

Oval, slightly raised plaque 2 to 5 cm, salmon-red, fine collarette scale at periphery. What is it?

A

Herald patch associated with Pityriasis rosea

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82
Q

Examining a patient you find: Fine scaling papules and plaques with marginal collarette. Dull pink or tawny. Oval, scattered, with characteristic distribution with the long axes of the oval lesions following the lines of cleavage in a “Christmas tree” pattern. What is the most likely diagnosis?

A

Exanthem associated with Pityriasis rosea

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83
Q

What is the treatment for Pityriasis Rosea?

A

-Spontaneous remission in 6 to 12 weeks or less
Symptomatic
- Oral antihistamines and/or topical antipruritic lotions for relief of pruritus
- Topical glucocorticoids
- May be improved by UVB phototherapy or natural sunlight exposure if treatment is begun in the first week of eruption.

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84
Q

Chronic disorder w/polygenic predisposition and triggering environmental factors (bacterial infection, trauma, drugs)

A

Psoriasis

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85
Q

What percent of psoriasis patients obtain arthritis?

A

10-25% of cases

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86
Q

What kind of immune response is psoriasis?

A

T-cell driven autoreactive immune response

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87
Q

Describe the epidemiology of Psoriasis. (ie. male or female; HLA?, peak incidence)

A
  • Peak incidence ~22.5 years-old
  • Male = Female
  • Polygenic trait(1 parent = 8%, 2 parents = 41%)
  • HLA Ags frequently associated
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88
Q

What are some common triggers for Psoriasis?

A 
Physical injury (Koebner’s phenomenon)
Infections
Stress
Drugs
ETOH
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89
Q

What is the pathogenesis of Psoriasis?

A

Keratinocyte cycle alteration (shortened cell cycle)

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90
Q

A psoriasis patient comes in for a follow up and you note plagues. What type of psoriasis does this patient have?

A

Chronic stable

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91
Q

A psoriasis patient comes in for a follow up and you note multiple small lesions. What type of psoriasis does this patient have?

A

Eruptive inflammatory

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92
Q

A male patient has been delaying coming into the clinic for fear he has some sort of weird skin cancer. You inspect the area and note:
-sharp margins, bright erythema, non confluent whitish or silvery scales
- lesions over random parts of his body
- notice that his nail beds and matrix
You ask further questions and discover he has been having arthritis symptoms. The patient also has positive Auspitz’s sign. What do inform the patient has?

A

Not cancer!!! But, Psoriasis with arthritis

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93
Q

A male patient has been delaying coming into the clinic for fear he has some sort of weird skin cancer. You inspect the area and note:
-sharp margins, bright erythema, non confluent whitish or silvery scales
- lesions over random parts of his body
- notice that his nail beds and matrix
You ask further questions and discover he has been having arthritis symptoms. The patient also has positive Auspitz’s sign. After informing the patient they don’t have cancer, what is the treatment?

A
  • Topical fluorinated glucocorticoids
  • Hydrocolloid dressing
  • Vitamin D (watch hypercalcemia) ± antibiotics
  • Scalp – mild (coal tar or ketoconazole), severe (Keralyt)
  • UV radiation
  • Coal tar
  • Methotrexate or Cyclosporine
  • Enbrel (etanercept), Remicade, Humira (TNF inhibitors)
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94
Q

List the Papulosquamous Diseases.

A
  1. Lichen Planus
  2. Pityriasis rosea
  3. Psoriasis
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95
Q

List the Desquamation conditions.

A
  1. Erythema multiform

2. Stevens-Johnson Syndrome & Toxic Epidermal Necrolysis

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96
Q

Reaction pattern of blood vessels in the dermis with secondary epidermal changes

A

Erythema Multiforme

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97
Q

What is the most common population that is affected by Erythema Multiforme?

A

-Age of onset - 50% under 20 years
-males > females
EM minor or *major (SJS & TEN)

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98
Q

What is the cause of Erythema Multiforme?

A

A cutaneous reaction to a variety of antigenic stimuli:

  • Infection - Herpes simplex (MC), Mycoplasma
  • Drugs; Sulfonamides, phenytoin, barbiturates, phenylbutazone, penicillin, allopurinol
  • Idiopathic (undetected Herpes or Mycoplasma)
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99
Q

Describe Erythema Multiforme.

A

Evolution of lesions over several days. May have history of prior episode. May be pruritic or painful, particularly mouth lesions.

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100
Q

Describe severe Erythema Multiforme.

A

fever, weakness, malaise may be present

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101
Q

A patient comes in complaining of a skin lesion that developed after 10 days. While inspecting the area, you discover a
papule about 2 cm large. You note vesicles and bullae in the center of the papule. It has a dull red color and is localized to hands and face. You note his mucous membranes – have erosions and ulcers. The lesions are overall bilateral and symmetric. What is the most likely diagnosis?

A

Erythema Multiforme

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102
Q

A patient comes in complaining of a skin lesion that developed after 10 days. While inspecting the area, you discover a
papule about 2 cm large. You note vesicles and bullae in the center of the papule. It has a dull red color and is localized to hands and face. You note his mucous membranes – have erosions and ulcers. The lesions are overall bilateral and symmetric. What is the best treatment?

A
  • Herpes, treat w/oral valacyclovir or famciclovir

- Severely ill patients, systemic glucocorticoids

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103
Q

Acute life-threatening mucocutaneous reaction characterized by extensive necrosis and detachment of the epidermis

A

Stevens-Johnson Syndrome & Toxic Epidermal Necrolysis

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104
Q

What are the causes of Stevens-Johnson & Toxic Epidermal Necrolysis?

A
  • Drug-induced (SJS – 50%, TEN – 80%) or idiopathic

- Cell-mediated cytotoxic reaction

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105
Q

What is the onset of Stevens-Johnson Syndrome & Toxic Epidermal Necrolysis?

A

Onset of symptoms; 1-3 weeks

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106
Q

What is the #1 cause of death for TEN?

A

Infection

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107
Q

What are some common risk factors for SJS and TEN?

A

SLE,
HLA-B12,
HIV/AIDS

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108
Q

What is the most common age of onset for SJS and TEN?

A

Any age, but most common in adults >40 years, M=F

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109
Q

A patient comes in complaining of a history of fever, malaise, arthralgias 1-3 days before rash. You examine the patient and discover:
mild to moderate skin tenderness, conjunctival burning/itching skin pain, burning sensation, paresthesia, and
mouth lesions that are painful/tender; and the patient reports photophobia. What is the most likely diagnosis?

A

SJS and TEN

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110
Q

A patient diagnosed with SJS and TEN have a rash that looks target-like. What stage of the condition are they in?

A

Prodrome

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111
Q

What is the treatment for SJS and TEN?

A 
Early diagnosis and withdrawal of suspected drug(s) are very important 
ICU
IV fluids and electrolytes
Systemic Glucocorticoids (early – ok, late – CI)
High dose IV immunoglobulins - early
Surgical debridement not recommended
Treat complications
Eyes w/erythromycin ointment
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112
Q

A patient comes in complaining of a history of fever, malaise, arthralgias 1-3 days before rash. You examine the patient and discover:
mild to moderate skin tenderness, conjunctival burning/itching skin pain, burning sensation, paresthesia, and
mouth lesions that are painful/tender; and the patient reports photophobia. What is the best treatment?

A
  • Early diagnosis and withdrawal of suspected drug(s) are very important
  • ICU
  • IV fluids and electrolytes
  • Systemic Glucocorticoids (early – ok, late – CI)
  • High dose IV immunoglobulins - early
  • Surgical debridement not recommended
  • Treat complications
  • Eyes w/erythromycin ointment
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113
Q

What is the likely cause of Bullous pemphigoid?

A

Autoimmune disorder

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114
Q

Which is more susceptible to Bullous pemphigoid: A 70 year old woman or 70 year old man?

A

Both are equally susceptible

Age of onset: >60, M=F

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115
Q

How is the blister formation in Bullous Pemphigoid believed to begin?

A

w/binding of IgG to bullous pemphigoid Ag, activation of complement, infiltrates of neutrophils and eosinophils

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116
Q

How does the prodromal eruption in Bullous Pemphigoid start?

A
  • urticarial, papular lesions and evolves in weeks to months to bullae
  • Initially no symptoms except moderate or severe pruritus; later, tenderness of eroded lesions
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117
Q

T/F Bullous Pemphigoid are only generalized skin lesions.

A

False: May be localized or generalized

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118
Q

A patient comes in complaining of an erythematous, papular and urticarial-type lesion. You inspect the area and find a
large, tense, firm-topped, oval lesion with what looks like serous fluid. What is the most likely diagnosis?

A

Bullous Pemphigoid

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119
Q

A patient comes in complaining of an erythematous, papular and urticarial-type lesion. You inspect the area and find a
large, tense, firm-topped, oval lesion with what looks like serous fluid. What would be some common areas to find this type of lesion?

A
  • Axillae
  • medial aspects of thighs,
  • groins,
  • abdomen;
  • flexor aspects of forearms;
  • lower legs (often first manifestation)
  • mucous membranes 10-35%
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120
Q

A patient comes in complaining of an erythematous, papular and urticarial-type lesion. You inspect the area and find a
large, tense, firm-topped, oval lesion with what looks like serous fluid. What treatment would you give this person?

A
  • Systemic prednisone with starting doses of 50 to 100 mg/d continued until clear
  • ± azathioprine
  • IVIG
  • Plasmapheresis
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121
Q

List the Acneiform Lesions.

A
  1. Acne vulgaris

2. Rosacea

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122
Q

How does Acne vulgaris manifest itself?

A

Mainfests itself as comedones, papulopustules, or nodules and cysts

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123
Q

What population is most susceptible to acne vulgaris?

A

Age of onset – Puberty;
10 to 17 years in females,
14 to 19 in males

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124
Q

What are some key factors for Acne Vulgaris?

A

follicular keratinization, androgens, and Propionibacterium acnes

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125
Q

T/F: People who like chocolate and fatty foods are more susceptible to acne.

A

False: Acne is not caused by any type of food

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126
Q

What seasons are worse for patients with acne?

A

Fall and winter

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127
Q

A patient comes in with comedones, papules and papulopustules. You inspect their face and note nodules and cysts—1 to 4 cm in diameter. What is the most likely diagnosis?

A

Acne vulgaris

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128
Q

A patient comes in with comedones, papules and papulopustules. You inspect their face and note nodules and cysts—1 to 4 cm in diameter. How would you treat this type of patient?

A

–Most often clears spontaneously

  • -Mild
  • Topical antibiotics (clindamycin and erythromycin)
  • Benzoyl peroxide gels (2%, 5%, or 10% )
  • Topical retinoids

–If moderate, add “cyclines”, (women – high dose estrogens+progesterone+antiandrogens)
Accutane??? (be aware of FDA restrictions - iPLEDGE)

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129
Q

Common chronic inflammatory acneiform disorder of the facial pilosebaceous units, increased reactivity of capillaries leading to flushing and telangiectasia

A

Rosacea

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130
Q

What population is more susceptible to Rosacea?

A
  • -Age of onset - 30 to 50 years;
  • -peak incidence between 40 and 50 years
  • -Celtic persons (skin phototypes I and II) but also southern Mediterraneans
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131
Q

What commonly occurs in men who suffer from Rosacea?

A

rhinophyma

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132
Q

How long should you instruct your Rosacea patient it will last?

A

Weeks to months

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133
Q

Episodic erythema, “flushing and blushing”

A

The Rosacea diathesis

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134
Q

Stage I Rosacea?

A

Persistent erythema with telangiectases

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135
Q

Stage III Rosacea?

A

Persistent deep erythema, dense telangiectases, papules, pustules, nodules; rarely persistent “solid” edema of the central part of the face

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136
Q

Stage II Rosacea?

A

Persistent erythema, telangiectases, papules, tiny pustules.

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137
Q

What are the two common “histories” you will hear from patients with

A
  1. Usually a history of episodic reddening of the face (flushing) with increases in skin temperature in response to heat stimuli in the mouth (hot liquids); spicy foods; alcohol
  2. Exposure to sun rosacea is often associated with solar elastosis and heat (such as chefs working near a hot stove) may cause exacerbations
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138
Q

A patient comes in and you notice pathognomonic flushing (red face); tiny papules and papulopustules about 2 to 3 mm, small < 1mm pustules and on the apex of the papule, but there are no comedones. What stage of what condition is this person in?

A

Early stage of Rosacea

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139
Q

What should you expect to see in a patient who is in late stage Rosacea?

A
  • Red facies and dusky-red papules and nodules
  • Scattered, discrete lesions.
  • Telangiectases
  • Marked sebaceous hyperplasia and lymphedema in chronic rosacea, causing disfigurement of the nose, forehead, eyelids, ears, and chin
140
Q

If a patient has chronic rosacea, what can you expect to see?

A

Marked sebaceous hyperplasia and lymphedema in chronic rosacea, causing disfigurement of the nose, forehead, eyelids, ears, and chin

141
Q

How would you manage a Rosacea patient?

A
  1. Rule out Staph infection, watch for Demodex infestation
  2. Recurrences are common, may disappear spontaneously
  3. Marked reduction or elimination of alcoholic and hot beverages may be helpful
142
Q

Rosacea Treatment

A

Topical
- Metronidazole gel or cream, 0.75%, twice daily or 1% daily

Systemic
- Minocycline or doxycycline(watch sunlight), 50 to 100 mg BID; oral metronidazole 500mg BID

143
Q

List the Verrucous Lesions.

A
  1. Seborrheic keratosis

2. Actinic (Solar) keratosis

144
Q

Most common of the benign epithelial tumors

A

Seborrheic keratosis

145
Q

What population is most at risk for seborrheic keratosis?

A

30 years and older

-Slightly more common and more extensive involvement in males

146
Q

A patient was previously diagnosed with seborrheic keratosis, but their skin lesion is not pruritic, but it is tender. What is going on?

A

Tender = infected

*it’s not supposed to be pruritic

147
Q

Where would you expect to see skin lesions in a patient with Seborrheic keratosis?

A

Distribution - Isolated lesion or generalized. Face, trunk, upper extremities

148
Q

Looking at a patient you see a small, 1- to 3-mm, barely elevated papule. On another area, you see a larger plaque with pigment, and it feels greasy. What is the most likely diagnosis?

A

EARLY Seborrheic keratosis

149
Q

What would you expect to see in a LATE Seborrheic keratosis patient?

A
  • plaque with warty surface and “stuck on” appearance
  • “greasy”
  • size from 1 to 6 cm
  • Flat nodule
  • Brown, gray, black, skin-colored
  • round or oval
150
Q

How would you treat Seborrheic keratosis?

A
  • Light electrocautery then cauterized
  • Curettage after light freezing w/cryospray (best)
  • Punch biopsy may be indicated
151
Q

Single or multiple, discrete, dry, rough, adherent scaly lesions occur on the habitually sun-exposed skin

A

Actinic (Solar) keratosis

152
Q

What population is more susceptible for Actinic (Solar) keratosis?

A
  • Middle age
  • MC in males
  • Occupation - Outdoor workers and outdoor sportspersons
153
Q

Considered “precancerous” SCC

A

Actinic (Solar) keratosis

154
Q

What is the pathogenesis of Actinic (Solar) keratosis?

A

Prolonged and repeated solar exposure in susceptible persons leads to cumulative damage to keratinocytes

155
Q

A patient comes in with papular lesions of all colors: Skin-colored, yellow-brown, brown and a reddish tinge one. You note they are rough, like coarse sandpaper. It is “better felt than seen” on palpation with your finger. The lesions are <1 cm, oval and round. What is the most likely diagnosis?

A

Actinic (Solar) keratosis

156
Q

What is the treatment for Actinic (Solar) keratosis?

A
  • Prevention – use sunscreens
  • May disappear spontaneously, but in general remain for years
  • Cryosurgery
  • 5-Flourouracil cream BID for 2-4 wks
  • Imiquimod BID wk for 16 wks
  • Facial peels - Trichloroacetic acid (5 to 10%)
  • Laser surgery
157
Q

Infestation of the scalp by the head louse, which feeds on the scalp and neck and deposits its eggs on the hair

A

Pediculosis capitis (Head Lice)

158
Q

What subspecies is responsible for Pediculosis capitis (head lice)?

A

subspecies Pediculus humanus capitis

159
Q

What population is most at risk for head lice?

A

Girls > boys,

Age of onset -3 to 11 years, but all ages

160
Q

How is head lice transmitted?

A

Shared hats, caps, brushes, combs; head-to-head contact

161
Q

How do head lice move?

A
  • Move by grasping hairs close to scalp

- can crawl up to 23 cm/day

162
Q

Where do the head lice lay their nits?

A

Within 1 to 2 mm of scalp

163
Q

What are nits?

A

Nits are ova within chitinous case

164
Q

Give the life cycle of the lice after they hatch (they hatch within the first week).

A

They pass through nymphal stages, growing larger and maturing to adults over a period of 1 week

165
Q

How many ova can a female head lice lay?

A

Females can lay 50 to 150 ova during a 16-day lifetime.

166
Q

Which sex (male or female) can last longer off the scalp?

A

Males can live longer off the scalp

167
Q

On average, how many lice does one patient have?

A

< 10

168
Q

What is Woods Lamp and how is it useful?

A

Live nits fluoresce with a pearly fluorescence; dead nits do not.

169
Q

A patient is having pruritis of the back and sides of the scalp, what diagnosis should you consider?

A

Pediculosis capitis (Head Lice)

170
Q

What is the treatment for head lice?

A

Avoid contact with possibly contaminated items
Vacuum area and disinfect (wash & dry) affected item, soak combs in rubbing alcohol or Lysol 2% solution for 1 h
Recommended
- Permethrin – OTC (1%) or prescription
(Elimite 5%) apply for 10 min, reapply in 7-10
days
- Malathione (Ovide) – apply to infected area for
8-12 hrs. (Lindane resistance). Not for children
< 6 mo.
Alternate
- Lindane 1% shampoo
- Ivermectin 0.8% lotion or shampoo
- Ivermectin 200 µg/kg, repeat in 10 days

171
Q

Pediculus humanus humanus

A

Species responsible for body lice

172
Q

Describe the habitat of body lice.

A

Live in seams of clothing; can survive without blood meal for up to 3 days.
Grab body hairs to feed.

173
Q
  • Lice and nits are found in clothing seams
A

Pediculosis Corporis (Body Lice)

174
Q

What are some risk factors to Pediculosis Corporis (Body Lice)?

A

Risk factors - Poor socioeconomic conditions, when clothing is not changed or washed frequently: poverty, war, natural disasters, indigence, homelessness, refugee-camp populations
Skin findings

175
Q

What is the proper treatment for Pediculosis Corporis (Body Lice)?

A

Bedding and clothing must be systematically decontaminated
Basic sanitation measures
Pyrethrins/pyrethroids or malathion for 8 to 24 h

176
Q

Infestation of hair-bearing regions, most commonly the pubic area, can be other areas

A

Pediculosis pubis (Pthiriasis)

177
Q

AKA – “crabs”

A

Pediculosis pubis (Pthiriasis)

178
Q

What species of “lice” is responsible for “crabs”?

A

Pthirius pubis

- Size 0.8 to 1.2 mm. Life span 14 days. Female lays 25 ova. Nits incubate for 7 days; nymphs mature over 14 days.

179
Q

What is the environment of “crabs”?

A

Mobility: adults can crawl 10 cm/day. Prefers a humid environment; tends not to wander.

180
Q

How is “crabs” transmitted?

A

Close physical contact: sexual exposure, sharing bed; possibly exchange of towels. Nonsexual transmission occurs in homeless persons who have pubic lice in hair on head and back.

181
Q

Lice appear as 1- to 2-mm, brownish-gray specks in hairy areas involved.

A

“Crabs”

182
Q

What is an indication of active infestation in “crabs”?

A

Nits attached to hair appear as tiny white-gray specks. Few to numerous.

Eggs at hair-skin junction indicate active infestation.

183
Q

What are some skin symptoms seen in “crabs”?

A
  • Often asymptomatic
  • Mild to moderate pruritis for months
  • Excoriations and 2ndary infections
  • Pt may notice “hair nodules”
  • Papular urticaria
  • Can infest eye lashes
184
Q

What is the treatment for “crabs”?

A
  • Treat patient and partners
  • Screen for other STD’s
  • Decontaminate clothing
  • Same as for head louse
185
Q

Sarcoptes scabiei var hominis

A

scabies

186
Q

How does Scabies get transmitted?

A

skin-to-skin contact, fomites

187
Q

What does the “scaby” do during the day?

A

lays eggs during day

188
Q

What does the “scaby” do during the night?

A

Tunnel into epidermis (“burrow/tunnel” usually at night

189
Q

In a patient that has scabies, the eggs hatch and migrate to the ———to mature

A

surface

190
Q

Does the female or male “scaby” burrow?

A

Female

The male falls off

191
Q

How do you identify Scabies?

A

ID by placing a drop of mineral oil over a burrow, scraped off with a no. 15 scalpel blade and placed on a microscope slide

192
Q

What is the treatment for Scabies?

A

Permethrin (Elimite) 5% Cream - applied to all areas of the body from the neck down. Wash off 8 to 12 h after application
Lindane 1% Lotion or Cream - applied thinly to all areas of the body from the neck down; wash off thoroughly after 8 h
Ivermectin (Stromectol)

193
Q

What is the treatment for Spider Bites?

A
  • Localized care
  • Elevation
  • Ice
  • Clean
  • Benadryl
  • Tylenol
  • Identify spider or most likely culprit
  • Call poison control or follow protocol
194
Q

List the Neoplasms.

A
  1. Basal Cell Carcinoma
  2. Kaposi Sarcoma
  3. Squamous Cell Carcinoma
  4. Melanoma
195
Q

MC cancer in humans

A

Basal Cell Carcinoma

196
Q

What is the cause of Basal Cell Carcinoma?

A

UVR, PTCH gene mutation

197
Q

What population is most susceptible to Basal cell carcinoma?

A
  • Age of onset - >40 years, M>F

- Distribution - Isolated single lesion; >90% occur in the face.

198
Q

Where do you search “danger sites” for Basal Cell Carcinoma?

A

Medial and lateral canthi, nasolabial fold, behind the ears

199
Q

What are the predisposing factors for Basal Cell Carcinoma?

A
  • Skin phototypes I & II
  • Heavy sun exposure as youth
  • X-ray therapy for facial acne
  • Ingestion of arsenic
200
Q

What is the treatment for Basal Cell carcinoma when it is detected early?

A

-Detect early – excision

201
Q

What is the treatment for Basal Cell carcinoma when it is detected late?

A
  • Detect late – excise but referral
  • Can use cryosurgery or electrosurgery for small lesions not in danger sites or on scalp
  • Radiation Tx
  • Topical 5-fluorurical or imiquimod
202
Q
  • Multifocal systemic tumor of endothelial cell origin

- Linked w/HHV-8

A

Kaposi Sarcoma

203
Q
  • Multifocal systemic tumor of endothelial cell origin

- Linked w/HHV-8

A

Kaposi Sarcoma

204
Q

CD4 count ≤ 500 µL (17%) + Kaposi Sarcoma `

A

Think HIV

-young males, rare in females

205
Q

What is the pathogenesis of Kaposi Sarcoma?

A
  • Derived from endothelium of blood/lymphatic microvasculature
  • Affects angiogenesis
  • Promotes own growth & growth of other cells
  • Not sure how HHV-8 induces proliferation
206
Q

How does Kaposi Sarcoma manifest?

A
  • Mucocutaneous lesions usually asymptomatic (may ulcerate and bleed)
  • Large lesion on palms/soles may limit function
  • LE lesions may produce severe pain if ulcerated/tumorous/edematous
  • Urethral/anal lesions = obstruction
  • Can affect Pulmonary
207
Q

What type of skin lesion does this describe?

  • eccymotic-like macule, evolve to patches, papules, plaques, nodules and tumors (violaceous, red, pink, tan then purple-brownish with greenish halo)
  • Palpable (firm to hard)
  • Can enlarge and become confluent
  • Lymphedema of LE
A

Kaposi Sarcoma

208
Q

Describe the distribution for Kaposi Sarcoma.

A
  • Widespread or localized
  • Almost always on hand/feet/legs and spreads centripetally
  • Trunk rare (except HIV)
  • Early face = HIV then to trunk
209
Q

What is the treatment of Kaposi’s Sarcoma?

A 
Control not cure
Limited intervention
   - Radiation
   - Cryo/laser/excisional surgery
   - Vincristine inj
Aggressive intervention
   - Single chemo: Adriamycin or Vinblastine
   - Combo chemo: Vincristine+Bleomycin+Adriamycin
210
Q

What is the treatment for Squamous Cell Carcinoma?

A

Topical chemotherapy - 5-Fluorouracil cream applied QD or BID, Imiquimod
Cryosurgery - Highly effective
Photodynamic therapy
Surgical excision - Has the highest cure rate but the greatest chance of causing cosmetically disfiguring scars

211
Q

Describe the skin lesion for squamous cell carcinoma.

A

Appears as a sharply demarcated, scaling, or hyperkeratotic macule, papule, or plaque

Solitary or multiple lesions are pink or red in color and have a slightly scaling surface, small erosions, and can be crusted (Bowen’s disease)

Red, sharply demarcated, glistening macular or plaque-like SCCIS on the glans penis or labia minora are called erythroplasia of Queyrat

212
Q

What does Melanoma arise from?

A
  • transformation of melanocytes at dermal-
    epidermal junction
    • dysplastic nevi
    • CNMN gone invasive (congenital…seen in young kids)
213
Q

What are the risk factors for Melanoma?

A 
Risk factors
   - CDKN2a mutation (cyclin dependent; regulates cell replication*) 
   - Skin types I &amp; II 
   - FHx or PHx 
   - UVR exposure (people with a lot of moles) 
   - Number (> 50) and size (> 5mm) of
     melanocytic nevi
   - Congenital nevi
214
Q

What are the risk factors for Melanoma?

A 
Risk factors
   - CDKN2a mutation (cyclin dependent; regulates cell replication*) 
   - Skin types I &amp; II 
   - FHx or PHx 
   - UVR exposure (people with a lot of moles) 
   - Number (> 50) and size (> 5mm) of
     melanocytic nevi
   - Congenital nevi
215
Q

What does ABCD stand for?

A 
Asymmetry
Borders
Colors
Diameter >~6mm
Elevation/Evolution/Enlargement
216
Q

What are the 4 major types of Melanoma?

A
  1. Lentigo maligna (5%)
  2. Spreading Superficial (70%)
  3. Acral-lentiginous (5-10%)
  4. Nodular (15%)
217
Q 
What does this describe?  
  - median age ~65
   - sunlight pathogenic
     factor
   - flat macule, border
     well defined,
    “geographic” shape
   - tan to brown/black
A

Lentigo maligna–the rates form of Melanoma

218
Q 
What does this describe? 
-age: 30-50 (~37)
   - upper back
   - elevated plaque
   - brown, dark brown,
     black, blue and red
A

Superficial spreading melanoma–the most common type of melanoma

219
Q 
What does this describe?
  - median age ~65
  - MC in Asians, AA
  - sole, palm; macule 
    w/focal papules/nodules
  - finger or toe nail; macule
    to papules/nodules
A

Acral-lentiginous (Acral = periphery)–one of the rarest melanomas

220
Q 
What does this describe? 
   - “middle life”
   - uniformly elevated
    “blueberry-like” nodule 
     or ulcerate or “thick” 
     plaque
   - “thundercloud”
A

Nodular Melanoma

221
Q

Does horizontal or vertical growth have a better prognosis?

A

Horizontal

222
Q

T/F: Nodular will most likely be vertical

A

True

223
Q

What is the treatment for Melanoma?

A
  • Excision
  • Malignant – pallative
  • Chemotherapy encompasses a large list of drugs (*dacarbazine/temozolomide, cisplatin, vindesine/vinblastine, fotemustine, taxol/taxotere)
224
Q

What is the treatment for Melanoma?

A
  • Excision
  • Malignant – pallative
  • Chemotherapy encompasses a large list of drugs (*dacarbazine/temozolomide, cisplatin, vindesine/vinblastine, fotemustine, taxol/taxotere)
225
Q

What are some skin cancer risk factors?

A 
Age (most > 40)
Race/Skin complexion
Sun exposure (watch certain medications)
Tanning Beds
# of Moles/freckles
Atypical nevi
Medical/Family Hx
Smoking
Immunosuppression
226
Q

What are some skin cancer warning signs?

A
  • Sore that does not heal
  • Spread of pigment from the border of a spot to surrounding skin
  • Redness or new swelling beyond the border
  • Change in sensation (itchiness, tenderness or pain)
  • Change in surface of a mole (scaling, oozing, bleeding or the appearance of a bump or nodule)
  • Mole that looks different from to other moles “ugly duckling” sign
227
Q

What is the onset of Alopecia aerata?

A

Age of onset - Young adults (<25 years); children are affected more frequently

228
Q

What are some associated symptoms with Alopecia aerata?

A

Hashimoto’s thyroiditis,
Vitiligo,
Myasthenia gravis (all are autoimmune)

229
Q

What is the treatment for Alopecia aerata?

A

-Trial of topical (usually not effective) or intralesional steroids (Triamcinolone)
-Systemic steroids/Cyclosporine?
PUVA
-May end just as suddenly as it started
-Can last months to years

230
Q

Common progressive balding that occurs through the combined effect of
(1) genetic predisposition, and (2) action of androgen (DHT) on scalp hair follicles

A

Androgenetic alopecia

231
Q

Male pattern baldness

A

Androgenetic alopecia

232
Q

When are the Androgenetic alopecia patients first effected/age of onset?

A
  • Males: May begin any time after puberty, as early as the second decade; often fully expressed in 40s.
  • Females: 40% occurs in the sixth decade
    Sex - Males&raquo_space; females
233
Q

What is the treatment for Androgenetic alopecia?

A
  • Finasteride - 1 mg PO QD
  • Topical Minoxidil 2 or 5% originally a bp medication
  • Women – Antiandrogens (Spironolactone)
  • Wigs, toupees, prosthetics; hair weaves
  • Hair transplantation
234
Q

Tinea Unguium/Onychomycosis offending agent

A

T. rubrum or mentagrophytes

235
Q

What kind of patients are more likely to have Tinea Unguium/Onychomycosis?

A

MC in immunocompromised patients and Diabetics

236
Q

A patient presents with: onycholysis, debris under nail; and thickening, crumbling. What is the most likely diagnosis?

A

Tinea Unguium/Onychomycosis

237
Q

How do you ID Tinea Unguium/Onychomycosis?

A

ID with scrapings w/KOH

238
Q

What is the treatment for Tinea Unguium/Onychomycosis?

A
  • Debridement and/or nail removal
  • Topical agents – Sporanox, Lamisil, Ciclopirox
  • Terbinafine – 250mg/d for 6 weeks for fingernails and 12-14 weeks for toenails
  • Itraconazole – 200mg/d for 6 weeks (fingernails and 12 weeks (toenails). Pulse dosing – 200mg BID for 1st 7 days of each month for 2 months (fingernails), 3-4 months for toenails
239
Q

What is Paronychia?

A

Acute infection of lateral or proximal nail fold. Usually associated with break in integrity of epidermis (e.g., hang nail), trauma, nail biting, manicure, dishwashing, chemical

240
Q

A patient walks in complaining of: throbbing pain, erythema, swelling, pain, with an abscess formation. Infection seems to be extending deeper, forming a felon. What is the likely diagnosis?

A

Paronychia

241
Q

What is the treatment of Paronychia?

A
  • Resolves spontaneously
  • Warm soaks (50% water/50% antibacterial soap 3-4xd)
  • Abscess needing I & D
  • po antibiotics?
242
Q

List the viral conditions.

A
  1. Condyloma acuminatum
  2. Infectious Exanthems (rash that appears after a fever)
  3. Herpes Simplex
  4. Molluscum contagiosa
  5. Verrucae
  6. Varicella-Zoster
243
Q

Caused by HPV (6,11) “genital warts”

A

Condyloma acuminatum

244
Q

What population is most susceptible to Condyloma acuminatum?

A

Young sexually active adults

245
Q

A 23 year old female comes into the office complaining of recent have itching, burning, bleeding, vaginal discharge, and dyspareunia. What is her most likely diagnosis?

A

Condyloma acuminatum

-Dormant for years

246
Q

What are the 4 clinical types of Condyloma acuminatum that occur?

A
  1. small papular
  2. cauliflower-floret lesions
  3. keratotic warts
  4. flat-topped papules/plaques
247
Q

With immunocompromised patients, what should you expect to see when inspecting for Condyloma acuminatum?

A

Lesions may be huge

248
Q

A fellow classmate is wondering why her preceptor was using Acetic acid during her OB/GYN rotation. How do you answer?

A

Acetic acid is helpful in:

visualizing lesions on the cervix and anus

when searching for Condyloma acuminatum

249
Q

How should you instruct your patient about preventing HPV?

A
  • Condoms
  • No therapy eradicates HPV
  • Vaccine
250
Q

There are 3 main ways to treat Condyloma acuminatum, describe them.

A
  1. External
    • Imiquimod, 5% cream
    • Podofilox 0.5% solution and gel
    • TCA or BCA 80-90%
    • Cryosurgery with liquid nitrogen
    • Laser removal
  2. Cervical
    • consultation
  3. Vaginal
    • Cryosurgery
    • TCA or BCA 80-90%
    • Podophyllin 10-25%
251
Q

What are Infectious Exanthems?

A
  • rash that appears after a fever

- Generalized cutaneous eruption

252
Q

You have an 18 year old patient come into the clinic with diffuse erythema, macular morbilliform, vesicular eruptions. He states that before this “rash” He had a fever, malaise, N/V/D, coryza, HA, and And pain.
What is the most likely offending agent which caused the condition?

A

Viral
Bacterial
Rickettsial
Parasitic

Age < 20

253
Q

You have an 18 year old patient come into the clinic with diffuse erythema, macular morbilliform, vesicular eruptions. He states that before this “rash” he had a fever, malaise, N/V/D, coryza, HA, and And pain.
What is the best way to manage this condition?

A

usually resolves <10d (reassurance)

antimicrobials if appropriate

254
Q

You have an 18 year old patient come into the clinic with diffuse erythema, macular morbilliform, vesicular eruptions. He states that before this “rash” he had a fever, malaise, N/V/D, coryza, HA, and And pain.
What is the most likely diagnosis?

A

Infectious Exanthems (rash that appears after a fever)

255
Q

How is Herpex Simplex transmitted?

A

Transmission – “shedding”, skin-skin, skin-mucosa

256
Q

When is Herpex Simplex latent?

A

in sensory ganglia after skin healing

you can spread herpes even though you are not shedding

257
Q

HSV-2

A

(urogenital)

258
Q

HSV-1

A

(oral)

259
Q

How do you diagnose Herpes Simplex?

A
  • Tzanck stain-looking for “multinucleate giant cells” (group vesicles) –PANCE
  • Serology
260
Q

A patient comes into the clinic. Your preceptor tells you the patient is has HSV–she asks you to describe the herpetic configuration. What do you say?

A
  • grouped small vesicles on erythematous base
  • superficial lesion-rupture early and erosion
  • crust and heal
261
Q

How do treat HSV?

A

Antivirals - “-cyclovirs”, “-ciclovirs”

Sunscreens may prevent outbreaks

262
Q

Self-limited epidermal viral infection, occurring in children, sexually active adults, IC

A

Molluscum contagiosum

263
Q

How does Molluscum contagiosum transmit?

A

skin-to-skin contact

spread by shaving,

264
Q

How long until a patient with Molluscum contagiosum undergoes regression?

A

Persist up to 6 months and then undergo spontaneous regression

265
Q

Who is susceptible to Molluscum contagiosum? And How do the lesions resolve?

A

HIV-Infected individuals - MC on the face, lesions resolve w/ART

266
Q

While inspecting a patient, you note: Papules (1 to 2 mm), nodules (5 to 10 mm) (rarely, giant) that are pearly white and skin-colored. They are round, oval, hemispherical, and umbilicated (centralized depression). At first glance, you think chicken pox. But then you remember it is actually what?

A

Molluscum contagiosum

267
Q

While inspecting a patient, you note: Papules (1 to 2 mm), nodules (5 to 10 mm) (rarely, giant) that are pearly white and skin-colored. They are round, oval, hemispherical, and umbilicated (centralized depression). At first glance, you think chicken pox. But then you remember it could be Molluscum contagiosum. If it is, what other term finding would be consistent with it?

A

Isolated single lesion; multiple, scattered discrete lesions; or confluent mosaic plaques

268
Q

How do you treat Molluscum contagiosum?

A
  • Supportive
  • 5% imiquimod cream applied qHS 3 times per week for up to 1–3 months
  • Tretinoin (Retin-A) qHS (at night)
  • Curettage
  • Cryosurgery
269
Q

Verruca Vulgaris

A

(Common Warts)

270
Q

Verruca Plantaris

A

(Plantar Warts)

271
Q

What is Verrucae caused by?

A

HPV

272
Q

How is Verrucae transmitted?

A

skin to skin contact

273
Q

A patient comes in with a wart, and does not want treatment, how long do you instruct this patient that it may last if they decide to leave the office without being treated?

A

often persist for several years

274
Q

What does this describe?

  • firm papules, 1 to 10 mm or rarely larger, hyperkeratotic, clefted surface, with vegetations
  • characteristic “red or brown dots”
A

Common warts

275
Q

What does this describe?
- early small, shiny, sharply marginated papule plaque with rough hyperkeratotic surface, studded with brown-BLACK dots

A

Plantar warts

276
Q

There is a characteristic to common warts that help identify it, what is it?

A
  • characteristic “RED or brown dots”
277
Q

How do you treat Verrucae ?

A
  • Salicylic acid and lactic acid in collodion
  • Imiquimod cream 3x/wk
  • Cryosurgery
  • CO2 laser-like genital warts
  • Hyperthermia for verruca plantaris (45°C for 20 mins, 2-3x week, ~16 Tx should be minimum)
  • Duct tape?
  • Numb the area, shave it and get down to the base and then put the steroid
278
Q

Primary infection – varicella or chicken pox

A

Varicella-Zoster

279
Q

Why is the chicken pox infection kind of a big deal?

A
  • Lifelong infection in sensory ganglia

- When immunity declines, VZV reactivates, erupts in a dermatomal pattern (zoster, or shingles)

280
Q

How is Varicella-Zoster transmitted?

A

via airborne droplets, direct contact

281
Q

What is the incubation of Varicella-Zoster virus?

A

14 days (range, 10 to 23 days)

282
Q

first lesion vesicle on erythematous base- “dewdrop on rose petal”

A

Varicella-Zoster

283
Q

A child is diagnosed with the varicella lesion. Where on the body would you expect to see these lesions?

A

Distribution: face and scalp, spreads inferiorly to trunk & extremities

284
Q

Your Derm preceptor ask you to explain the zoster prodromal symptoms. How do you respond?

A

Prodromal symptoms – burning, tingling

285
Q

What is the treatment of Varicella-Zoster?

A
  • Vaccine available (Varivax)
  • Oral antihistamines
  • Antivirals -cyclovirs
  • can give Hydroxazine for the itching
286
Q

List the Bacterial Infections

A
  1. Cellulitis/Erysipelas

2. Impetigo

287
Q

What are the 2 types of Impetigo?

A
  1. Bullous Impetigo

2. Nonbullous Impetigo

288
Q

How should you go about treating non-bullous impetigo?

A
  • no vesicles here

- Topical tx

289
Q

How should you go about treating bullous impetigo?

A

Go systemic

290
Q

How do you treat Impetigo?

A

Topical - Mupirocin ointment. Apply 2x daily to involved skin and to nares for 7 to 10 days.

Systemic antibiotic

Watch for MRSA

Stop the scratching; always wash your hands

291
Q

How do you prevent Impetigo?

A
  • Daily bath,
  • Benzoyl peroxide wash (bar).
  • Check family members for signs of impetigo.
  • Ethanol or isopropyl gel for hands and/or involved sites
292
Q

While inspecting a patient, you note:

Vesicles and bullae containing clear yellow or slightly turbid fluid, with surrounding erythema. One of the lesions was decompressed. You remove the roof of bulla and see a shallow moist erosion forming.

What is the most likely diagnosis?

A

Bullous Impetigo

293
Q

Superficial infections of the epidermis

A

Impetigo

294
Q

Crusted erosions or ulcers

A

Ecthyma

295
Q

A patient is diagnosed with Impetigo. What is the most likely offending agent causing this condition?

A

S. aureus most commonly; GAS

296
Q

Primary infections of Impetigo commonly infect what age group?

A

Children

297
Q

Secondary infections of Impetigo commonly infect what age group?

A

Any age group

298
Q

Epidermolytic toxin A-gene S. aureus (staphylococcal scalded-skin syndrome)

A

Bullous impetigo

299
Q

T/F: Impetigo is an associated with Atopic Dermatitis

A

True

300
Q

How long does Impetigo last?

A

days to weeks

301
Q

How do you treat Cellulitis/Erysipelas?

A
  • Supportive
  • Antibiotics
    • Ceftriaxone, Augmentin, Doxy, Cipro
    • If MRSA, Vancomycin or Linezolid
  • Surgery
302
Q

What is this describing?

  • inflammation of the connective/subcutaneous
    tissues
  • Lesions: hard to palpation, extremely painful
  • Cause: Staph & GAS MC
A

Cellulitis

303
Q

What is this describing?

  • superficial cutaneous cellulitis skin infection w/marked dermal lymphatic involvement
    • Lesions: painful, bright red, raised, edematous,
      indurated plaque w/red borders, sharply marginated
    • Most likely caused by GAS
      Look for warm, bright pink, indurated*
A

Erysipelas

304
Q

What are some of the offending agents of cellulitits/erysipelas?

A

Adults: S. aureus, GAS.

Children: H.influenzae type b (Hib), GAS, S. aureus. Less commonly - Group B streptococci (GBS), pneumococci

Dog, Cat or Human Bites: Pasturella and Staph ; human is Icanella

305
Q

What is this description:

  • Red, hot, edematous and shiny plaque, and very tender area of skin of varying size
  • Borders usually sharply defined, irregular, and slightly elevated; bluish purple color with H. influenzae
  • Vesicles, bullae, erosions, abscesses, hemorrhage, and necrosis may form in plaque
  • Lymphangitis
A

cellulitits/erysipelas

306
Q

In children, what is the distribution of cellulitits/erysipelas?

A

cheek, periorbital area, head and neck

307
Q

In adults, what is the distribution of cellulitits/erysipelas?

A

lower leg (MC), arm, trunk, face

308
Q

Erysipelas

A
  • Tinea infection
  • Tinea pedis
  • Person scratched it
  • May be indurated and hot
309
Q

Erysipelas can originate from what eye condition?

A

From conjunctivitis

310
Q

List the fungal conditions.

A
  1. Candidiasis
  2. Pityriasis (tinea) versicolor
  3. Tinea corporis
  4. Tinea pedis (Athlete’s foot)
311
Q

Agent – Candida albicans causes what?

A

Candidiasis

312
Q

What are the types of Candidiasis?

A
  1. Cutaneous
  2. Oropharyngeal
  3. Chronic mucocutaneous
  4. Genitalia
313
Q

What lab is very useful for evaluating Candidiasis?

A

KOH prep

314
Q

If a patient is suffering from cutaneous candidiasis, how should their symptoms present?

A
  • erythema, pruritis
315
Q

If a patient is suffering from Oropharyngeal candidiasis, how should their symptoms present?

A
  • AH HA!!!! often asymptomatic!!!!

- burning or pain?, odynophagia

316
Q

If a FEMALE patient is suffering from genital candidiasis, how should their symptoms present?

A

pruritis, white discharge, burning, erythema (F)

317
Q

If a MALE patient is suffering from genital candidiasis, how should their symptoms present?

A

erythema, papules, removable curdlike material (M)

318
Q

If a patient is suffering from Chronic mucocutaneous candidiasis, how should their symptoms present?

A
  • erythema, pruritis
  • often asymptomatic
  • burning or pain?, odynophagia
319
Q

What is the treatment for Candidiasis?

A
  1. Topical agents
    - Topical Nystatin or Imidazole
    - Butoconazole or Clotrimazole cream
    - “azole” suppository
  2. Oral agents
    - Clotrimazole
    - Itraconazole
    - Ketoconazol
    - Fluconazole
    - Diflucan*
320
Q

Chronic asymptomatic scaling epidermomycosis

A

Pityriasis (tinea) versicolor

321
Q

How is Pityriasis (tinea) versicolor characterized?

A

by well-demarcated scaling patches with variable pigmentation, occurring most commonly on the trunk

322
Q

What is the age of onset for Pityriasis (tinea) versicolor?

A

YOUNG adults

323
Q

What are some Predisposing factors to Pityriasis (tinea) versicolor?

A
  • high temperatures/relative humidity,
  • oily skin
  • hyperhidrosis
  • hereditary factors
  • glucocorticoid treatment and immunodeficiency.

Application of lipids such as cocoa butter predisposes young children to PV

324
Q

Instructing a patient being diagnosed with Pityriasis (tinea) versicolor, where should you tell her this rash will show up on her body?

A

Distribution -

Upper trunk, 
upper arms, neck, 
abdomen, 
axillae, 
groins, 
thighs, 
genitalia
325
Q

KOH prep – Spaghetti & meatballs

A

Pityriasis (tinea) versicolor

326
Q

Wood’s lamp – blue-green fluorescence

A

Pityriasis (tinea) versicolor

327
Q

What is the treatment for Pityriasis (tinea) versicolor?

A

-Selenium sulfide (2.5%)/ketoconazole shampoo - apply daily to affected areas for 10 to 15 min, followed by shower, for 1 week

-Terbinafine (Lamisil) 1% solution – apply BID for 7 days
“azole” creams - Apply QD or BID for 2 weeks

328
Q

What is the treatment for Pityriasis (tinea) versicolor?

A

-Selenium sulfide (2.5%)/ketoconazole shampoo - apply daily to affected areas for 10 to 15 min, followed by shower, for 1 week

-Terbinafine (Lamisil) 1% solution – apply BID for 7 days
“azole” creams - Apply QD or BID for 2 weeks

329
Q

Dermatophyte infections of the trunk, legs, arms, and/or neck, excluding the feet, hands, and groin

A

Tinea corporis

330
Q

What population of people are most susceptible to Tinea corporis?

A

Occupation - Animal workers

331
Q

T. rubrum most common (ruby red)

A

Tinea corporis causative agent

332
Q

How is Tinea corporis transmitted?

A

Autoinoculation from other parts of the body, contact with animals or contaminated soil

333
Q

What are some symptoms associated with Tinea corporis?

A

Symptoms - Often asymptomatic, mild pruritus

334
Q

What is this describing?

  • Small to large scaling, sharply marginated plaques with or without pustules or vesicles, usually at margins
  • Peripheral enlargement and central clearing produces annular configuration with concentric rings or arcuate lesions; fusion of lesions produces gyrate patterns
  • Single and occasionally scattered multiple lesions
  • Target like lesion
  • Don’t confuse with lyme disease
  • Persists longer it will lighten up
  • Looks like person has scratch marks all over
A

Tinea corporis

335
Q

What is the treatment for Tinea corporis

A
  • “-azoles”
  • Preparation is applied BID to involved area and at least 1 - 2 week after lesions have cleared
  • Apply at least 3 cm beyond advancing margin of lesion
336
Q

Dermatophytic infection of the foot that can spread to other sites and more common in males

A

Tinea pedis (Athlete’s foot)

337
Q

What population is at risk for Tinea pedis (Athlete’s foot)?

A

Age of onset - Late childhood or young adult life.

Most common, 20 to 50 years

Sex - Males > females

338
Q

What are some predisposing factors of Tinea pedis (Athlete’s foot)?

A

Predisposing factors - Hot, humid weather; occlusive footwear; excessive sweating

339
Q

How does Tinea pedis (Athlete’s foot) get transmitted?

A

Transmission - Walking barefoot on contaminated floors. Arthrospores can survive in human scales for 12 months

340
Q 
What are the 2 types of Interdigital Type
Tinea pedis (Athlete’s foot)?
A

Two patterns:
1. dry scaling
2. maceration, peeling, fissuring of toe webs
- Hyperhidrosis common
- Most common site: between fourth and fifth
toes
- Infection may spread to adjacent areas of feet

341
Q 
What type of Type
Tinea pedis (Athlete’s foot) does this describe?
  • Well-demarcated erythema with minute papules on margin, fine white scaling, and hyperkeratosis (confined to heels, soles, lateral borders of feet)
    Distribution: Sole, involving area covered by a ballet slipper. One or both feet may be involved with any pattern; bilateral involvement more common
A

Moccasin Type

342
Q 
What type of Type
Tinea pedis (Athlete’s foot) does this describe?
  • Well-demarcated erythema with minute papules on margin, fine white scaling, and hyperkeratosis (confined to heels, soles, lateral borders of feet)
    Distribution: Sole, involving area covered by a ballet slipper. One or both feet may be involved with any pattern; bilateral involvement more common
A

Moccasin Type

343
Q

Describe the Inflammatory/Bullous Type of Tinea pedis (Athlete’s foot)

A
  • Vesicles or bullae filled with clear fluid. Pus usually indicates secondary S. aureus infection or group A streptococcus
344
Q 
What type of Type
Tinea pedis (Athlete’s foot) does this describe?
  • Extension of interdigital tinea pedis onto dorsal and plantar foot. Usually complicated by bacterial infection
A

Ulcerative Type

345
Q 
What type of Type
Tinea pedis (Athlete’s foot) does this describe?
  • Extension of interdigital tinea pedis onto dorsal and plantar foot. Usually complicated by bacterial infection
A

Ulcerative Type

346
Q

What is the treatment of Tinea pedis (Athlete’s foot)?

A

Prevention – wear shower shoes, wash w/benzoyl peroxide bar

Antifungals “-azoles”

Clin Med II (9 decks)

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